Context. Vitamin D is essential for skeletal and nonskeletal health and prolonged deficiency results in infantile rickets and adult osteomalacia. The aim of this study is to determine 25(OH) VitD and iPTH status in pregnancy and to evaluate the effects of monthly 100.000 IU dose of vitamin D supplementation.Materials and Methods. In a double blind trial of vitamin D supplementation in pregnant Iranian women, vitamin D3 (cholecalciferol , 100/00 IU/month) was administered to 25 women and placebo to 25 controls during the last trimester. The two groups had similar distributions of maternal age, height, gravity, weight and age of gestation. Hydroxycholcalciferol and iPTH were measured in mothers at 27 weeks and at delivery. Cord blood was used to assess the same parameters.Results. Comparing the data final maternal 25 -hydroxyvitamin D levels were significantly higher in the supplemented group versus control group (61.45±30 ng/mL versus 29.4±16 ng/mL); P ≤ 0.001.Cord 25hydroxyvitamin D levels were significantly higher in supplementation group in comparison to control group (52 ± 40.5 ng/mLversus 36±21.3 ng/mL); P<0.005.Conclusion. Administration of 100/000 IU/monthly of vitamin D3 in the last trimester significantly increased 25(OH) VitD to high normal concentration. However, even with supplementation, only of mother and of newborn had serum 25(OH) VitD greater than 30 ng/mL a small percentage of women and babies were vitamin D sufficient. According to data of study we propose 100/000 IU monthly is safe for pregnant women.

Background: Despite existing evidence regarding the role of testosterone as a protective factor for the kidney function in male adults, there are conflicting and inconclusive results on the influence of testosterone deficiency on developing chronic kidney disease (CKD).Objective: This study aimed to investigate the incidence and hazard ratio of CKD among male adults with low testosterone levels compared to controls with normal testosterone levels. Materials and Methods: During a 15-year follow-up study, a total of 1277 eligible male adults aged 20-80 year consisting of 605 males with low testosterone levels (< 350 ng/dL) and 672 controls with normal levels participating in the Tehran Lipid andGlucose Study were recruited. Cox's proportional hazards models were applied to estimate hazard ratios of CKD between the groups after adjusting for confounders. Results:The total cumulative incidence rate of CKD at the median follow-up time of approximately 11.2 years was 21/1000 (95% CI: 18/1000, 25/1000) and 18/1000 (95% CI: 16/1000, 22/1000) in the low and normal testosterone groups, respectively (P = .2). The multivariate Cox model adjusted for age, body mass index, dyslipidemia, hypertension, diabetes, and smoking showed that HR of developing CKD in the male adults with low testosterone levels was significantly higher than those with normal levels (HR = 1.38; 95% CI: 1.05, 1.80). Discussion and conclusion:This study shows a higher hazard ratio of CKD progression in male adults with hypogonadism compared to those with normal levels in their later life. Therefore, timely diagnosis and treatment of kidney diseases in hypogonadal men can prevent the morbidity and mortality from CKD.

Background: The association between low testosterone concentration and increased risk of hyperglycemia in men has been demonstrated in observational and interventional studies. However, considering a variety of confounding factors, limited population-based studies have so far been conducted. Also, no information is available regarding the effect of testosterone on progressive development of dysglycemia. Objective: To examine the effect of total testosterone on development of pre-diabetes/diabetes in normoglycemic middle-aged and older men. Materials and Methods: Data were obtained from the Tehran Lipid and Glucose Study, a community-based prospective cohort of an Iranian population. Analyses were conducted on 903 normoglycemic eligible men aged 30-70 years. An illness-death model was applied to estimate the probabilities of three transitional phases of normoglycemia?diabetes, normoglycemia?pre-diabetes, and pre-diabetes?diabetes. Results: Over a median follow-up of 12 years, 0.9% individuals developed diabetes. Per unit increase (ng/mL) in testosterone concentration, the transition rate from normoglycemia to pre-diabetes decreased by 6% [hazard ratios (HRs): 0.94 (95% confidence interval (CI): 0.90, 0.99)]. However, no effect for testosterone on the progression of diabetes from normoglycemia or pre-diabetes was observed [HRs: 0.79 (95% CI: 0.44, 1.41) and 0.98 (95% CI: 0.84, 1.16), respectively]. High body mass index was a strong predictor of hyperglycemia within all transitions. Discussion: Independent of major confounding factors, low testosterone was associated with normoglycemia progression to prediabetes, but not with pre-diabetes to diabetes, which might indirectly highlight the stronger impact of other risk factors after occurrence of pre-diabetes. Conclusion: Low testosterone concentrations in men are associated with progression from normoglycemia to pre-diabetes, but not from pre-diabetes to diabetes.